Aging and OA

What is the greatest risk factor for OA? Getting older. Aging does not directly cause OA, or everyone would have it at a certain age, but 50 percent of people older than 65 do have it. Genes, prior injury or other factors increase the risk, and aging itself contributes to the development of OA because of the changes that occur to the joint over time, says Richard Loeser Jr., MD, program director of both the Translational Science Institute and the Sticht Center on Aging at Wake Forest University School of Medicine in Winston-Salem, N.C. “There are other factors involved in actually causing it, such as obesity, joint injury and genetics,” he says. “The [aging-related] changes in the joint contribute to its development.”

One piece of the puzzle appears to be the long life of chondrocytes, the cells that make up cartilage. Unlike other cells, which repair and regenerate themselves, chondrocytes have very little turnover. That fact, according to Dr. Loeser, “makes tissue like cartilage uniquely susceptible to the effects of reactive oxygen species,” also known as “free radicals.” Free radicals can cause significant damage to cell structures.

Another source of damage is excessive mechanical stress on the joint. But, he adds, OA is related to abnormal mechanical stress caused by misaligned joints or injury, not normal, everyday loading on joints.

So why don’t all older adults get OA? Researchers don’t know, Dr. Loeser says. He points to a Dutch study of more than 80 adults, ages 89 to 91, which found that 63 percent had no hip OA, 51 percent had no knee OA, and 29 percent had no hand OA. Who was least likely to develop OA? Men, people with a normal BMI, those with no family history of nodal OA in the hands, those with low innate production of two types of interleukin proteins, and – perhaps counterintuitively – people with a history of heavy work.

Although we can’t halt the aging process, researchers are working on understanding the biology of OA as it relates to aging, such as how oxidative stress contributes to the degenerative disease, and how abnormal mechanical stress plays a role. “We know a lot more now about the biology of the disease and the changes occurring in the joint tissues in terms of aging and how they would predispose the joint to OA, but we still don’t know the best way to intervene,” says Dr. Loeser.

“The message we’re trying to get out is that OA is not simply a degenerative disease of aging,” he says. “It’s an active, inflammatory disease. Your joint is not like an automobile that wears out over time.”